The parallel measurement of serum antibodies to the hepatitis G virus
(anti-HGV) and of viremia (HGV-RNA) should improve our understanding o
f HGV transmission by coagulation factor concentrates. The aim of this
study was to assess the relationship between HGV, the type of concent
rate infused, and liver disease in multitransfused hemophiliacs. To th
is end, anti-HGV and HGV-RNA were evaluated by an enzyme-linked immuno
sorbent assay and a nested-polymerase chain reaction assay in patients
treated lifelong with nonvirus-inactivated plasma-derived concentrate
s (n = 128), virus-inactivated concentrates (n = 33), or recombinant f
actors (n = 7), and in 200 regular blood donors. The prevalence of ser
um HGV-RNA and anti-HGV was higher in the recipients of nonvirus-inact
ivated factors than in blood donors (HGV-RNA: 9% v 1.5%, P = .002; ant
i-HGV: 32% v 5%, P < .0001). In the recipients of virus-inactivated co
ncentrates the prevalences of these markers were similar to those in b
lood donors (HGV-RNA: 3% v 1.5%; anti HGV: 15% v 5%). The prevalence o
f either marker in the recipients of nonvirus-inactivated concentrates
was higher than in the recipients of virus-inactivated factors (39% v
18%, P = .04). The former group had serum hepatitis C virus (HCV) RNA
or anti-HCV more frequently than the latter group (HCV-RNA: 86% v 15%
, P < .0001; anti-HCV: 96% v 18%, P < .0001). Serum alanine aminotrans
ferase was persistently high in 83 (81%) patients with HCV-RNA alone,
in 8 (89%) with HCV/HGV coinfection, and in none of the three patients
with HGV-RNA only, Thus, HGV infection in hemophiliacs is more common
than previous studies of HGV-RNA prevalence have suggested, but it re
solved in most cases and caused chronic viremia only in a small number
of patients, without biochemical evidence of persistent liver damage.
(C) 1997 by The American Society of Hematology.